In equine models of intestinal ischaemia and endotoxaemia, antiplatelet drugs are generally ineffective, whereas Dextran 70 shows utility for thromboembolic colic.
Should not yet alter equine protocols; leaves open prospective RCTs of Dextran 70.
Summary Activation of platelets is the key step in the formation of macroscopic thrombi and emboli and in micro‐thromboembolism associated with disseminated intravascular coagulation (DIC). Macroscopic thrombosis may compromise the blood supply of the gut. Strangulation or infarction of the gut, from whatever cause, commonly result in endotoxaemia, DIC and multiple organ failure. Equine platelets may be activated physiologically by a wide range of agonists. Information is now emerging about the receptor populations and intracellular signalling pathways of equine platelets. Less is known about platelet‐vessel wall interactions in the horse or the mechanisms of platelet activation in endotoxaemia. Antiplatelet drugs have been disappointing in endotoxaemia, possibly because of the relative unimportance of thromboxane production in the activation of equine platelets. Dextran 70, however, is a useful treatment of thromboembolic colic and the mechanism of action is now beginning to be understood.
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Richard J. Evans (1992) studied this question.
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